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'''VE (nerve agent)'''
{{short description|Chemical compound and nerve agent}}
{{Use dmy dates|date=October 2023}}


VE is a [[nerve agent]] that belongs to the [[V-series]] of nerve gases. It is a potent [[cholinergic]] agent that inhibits the breakdown of [[acetylcholine]] in the [[synapse]], leading to a buildup of the neurotransmitter and overstimulation of the [[nervous system]].
[[File:VE-2D-skeletal.png|thumb|Chemical structure of VE nerve agent]]


== History ==
'''VE''' is a [[nerve agent]] of the [[V-series]] of [[organophosphorus]] compounds. It is closely related to the more well-known [[VX (nerve agent)|VX]] nerve agent. Like other V-series agents, VE is a potent [[acetylcholinesterase inhibitor]], leading to the accumulation of [[acetylcholine]] in the [[synaptic cleft]] and causing continuous stimulation of [[muscle]]s, [[gland]]s, and [[central nervous system|central nervous system]].


VE was first synthesized in the 1950s as part of a series of nerve agents developed by the [[Soviet Union]]. The V-series of nerve agents, which also includes [[VX (nerve agent)|VX]] and [[VR (nerve agent)|VR]], were designed to be more potent and persistent than the [[G-series]] nerve agents such as [[sarin]] and [[soman]].
==Chemical properties==
VE is an [[organophosphate]] compound with the chemical formula C<sub>11</sub>H<sub>26</sub>NO<sub>2</sub>PS. It is a [[colorless]] to [[amber]]-colored [[liquid]] at room temperature. The compound is [[odorless]] and [[tasteless]], making it difficult to detect without specialized equipment.


== Mechanism of Action ==
==Mechanism of action==
VE acts by inhibiting the enzyme [[acetylcholinesterase]], which is responsible for breaking down the neurotransmitter [[acetylcholine]] in the [[synaptic cleft]]. When acetylcholinesterase is inhibited, acetylcholine accumulates, leading to continuous stimulation of [[muscle]]s and [[nerve]]s. This results in [[muscle paralysis]], [[respiratory failure]], and potentially [[death]] if not treated promptly.


VE inhibits the enzyme [[acetylcholinesterase]], which is responsible for breaking down acetylcholine in the synapse. This leads to a buildup of acetylcholine, causing overstimulation of the nervous system. Symptoms of VE poisoning include [[muscle spasms]], [[respiratory failure]], and [[seizures]]. In severe cases, exposure to VE can be fatal.
==Toxicity and symptoms==
Exposure to VE can occur through [[inhalation]], [[ingestion]], or [[skin contact]]. Symptoms of exposure include [[miosis]] (constricted pupils), [[rhinorrhea]] (runny nose), [[dyspnea]] (difficulty breathing), [[muscle twitching]], and [[convulsions]]. Severe exposure can lead to [[coma]] and [[death]].


== Treatment ==
==Treatment==
The primary treatment for VE exposure is the administration of [[atropine]] and [[pralidoxime]]. Atropine works by blocking the effects of acetylcholine at [[muscarinic receptors]], while pralidoxime reactivates acetylcholinesterase. [[Diazepam]] may also be used to control [[seizures]].


Treatment for VE exposure involves the administration of [[atropine]] and [[pralidoxime]], which help to counteract the effects of the nerve agent. Immediate medical attention is crucial, as the effects of VE can be rapid and severe.
==History and development==
The V-series nerve agents, including VE, were developed in the 1950s by the [[United Kingdom]] and later by the [[United States]] and other countries. These agents were designed to be more persistent and potent than earlier nerve agents like [[sarin]] and [[tabun]].


== See Also ==
==Related pages==
* [[VX (nerve agent)]]
* [[Sarin]]
* [[Tabun]]
* [[Nerve agent]]


* [[Chemical warfare]]
==References==
* [[Nerve gas]]
* {{cite book |last=Sidell |first=Frederick R. |title=Medical Aspects of Chemical and Biological Warfare |publisher=Office of The Surgeon General, Department of the Army, United States of America |year=1997 |isbn=978-0-16-045135-3}}
* [[Organophosphate poisoning]]
* {{cite journal |last=Emsley |first=John |title=The Shocking History of Phosphorus |journal=Nature |volume=393 |issue=6682 |pages=127–128 |year=1998 |doi=10.1038/30164}}
 
== References ==
 
<references />


[[Category:Nerve agents]]
[[Category:Nerve agents]]
[[Category:Chemical weapons]]
[[Category:Organophosphates]]
[[Category:Toxicology]]
{{Chemical weapons}}
{{Toxicology-stub}}

Revision as of 12:00, 9 February 2025

Chemical compound and nerve agent



Chemical structure of VE nerve agent

VE is a nerve agent of the V-series of organophosphorus compounds. It is closely related to the more well-known VX nerve agent. Like other V-series agents, VE is a potent acetylcholinesterase inhibitor, leading to the accumulation of acetylcholine in the synaptic cleft and causing continuous stimulation of muscles, glands, and central nervous system.

Chemical properties

VE is an organophosphate compound with the chemical formula C11H26NO2PS. It is a colorless to amber-colored liquid at room temperature. The compound is odorless and tasteless, making it difficult to detect without specialized equipment.

Mechanism of action

VE acts by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synaptic cleft. When acetylcholinesterase is inhibited, acetylcholine accumulates, leading to continuous stimulation of muscles and nerves. This results in muscle paralysis, respiratory failure, and potentially death if not treated promptly.

Toxicity and symptoms

Exposure to VE can occur through inhalation, ingestion, or skin contact. Symptoms of exposure include miosis (constricted pupils), rhinorrhea (runny nose), dyspnea (difficulty breathing), muscle twitching, and convulsions. Severe exposure can lead to coma and death.

Treatment

The primary treatment for VE exposure is the administration of atropine and pralidoxime. Atropine works by blocking the effects of acetylcholine at muscarinic receptors, while pralidoxime reactivates acetylcholinesterase. Diazepam may also be used to control seizures.

History and development

The V-series nerve agents, including VE, were developed in the 1950s by the United Kingdom and later by the United States and other countries. These agents were designed to be more persistent and potent than earlier nerve agents like sarin and tabun.

Related pages

References

  • Frederick R.,
 Medical Aspects of Chemical and Biological Warfare, 
  
 Office of The Surgeon General, Department of the Army, United States of America, 
 1997, 
  
  
 ISBN 978-0-16-045135-3,
  • Emsley, John,
 The Shocking History of Phosphorus, 
 Nature, 
 1998,
 Vol. 393(Issue: 6682),
 pp. 127–128,
 DOI: 10.1038/30164,